nervous system Flashcards by Mckenna Yarrows

what are the signs and symptoms of parkinsons disease

tremor (pill rolling)
bradykinesia (slow movement, short steps)
rigidity (stiff ms)
postural instability
balance
automatic movements
speech (changes in pace and intensity, monotone)
writing (challening, small text)

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etiology of parkinsons

genetics and toxins

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what is parkinsons disease

progessive neurologic condition that affects movement

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parkinsons risk factors

middle aged-old people
men are higher risk
relatives
exposure to toxins and pesticides

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predromal stage of parkinsons symptoms

REM sleep disorder
depression
constipatoin
anxiety
hypoxia (decreased smell)
daytime sleepiness

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early stage parkinson symptoms

bradykinesia, rigidity,
fatigue
tremor
pain
apathy
mild cognitive impairments

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mid stage parkinsons symptoms

fluctuations
dyskinesias
urinary symptoms
orthostatic hypotension
axial deformities
visual hallucinations

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late stage parkinsons symptoms

dysphagia
falls
dementia

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changes in the brain during parkinsons disease

gradual loss of cells in the substantia nigra (production of dopamine)
dopamine stimulates smooth muscle contractions/pathways
decreased dopamine leads to ms rigidty and tremors
prescense of lewy bodies in the brain (sticky proteins associated w dementia)

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PT implications of parkinsons disease

cognitive change
depression and emotional change
dysphagia
sleep disorders
bladder incontinence
constipation
orthostatic changes
fatigue
pain

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what is myasthenia gravis

an autoimmune neurologic disorder that is the most common primary disorder of neuromuscular transmission

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what are some symptoms of myasthenia gravis

fluctuating weakness and rapid fatigue of skeletal muscle – improves with rest

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what muscles are most affected with myasthenia gravis

muscles with small motor units such as ocular
severe cases - diapragm and intercostals

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what percent of patients with MG have coexistent hyperthyroidism

about 5%

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what percent of MG pts have a maternal relative with an autoimmune disease

about 30

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risk factors of Myasthneia gravis

young women 20-30yrs
men>50 years

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what happens in the presynaptic pathogensis of MG

number and size of vesicles are normal

what happens in the postsynaptic pathogensis of MG

muscle endplate shows sparse, shallow, and abnormally wide or absent synaptic cleft; fewer ACh receptors

electrophysiology of MG

postsynaptic membrane has decreased response to acetylcholine = lack of contractibility

signs and symptoms of MG

visual
muscle
thymus
flare ups
remission

muscular symptoms of MG

fatigue and weakness may vary rapidly in intensity over hours, days, and weeks
facial, swallowinf, neck, and limb muscles are involves

visual symptoms/signs of MG

extraocular muscle=ptosis or dropping eyelinds and diplopia or double vision

thymus symptoms of MG

abnormalities associated but nature of association is unclear

how to diagnosis MG

neurologic exam
blood test
ice test
nerve conduction test
electromyogram

treatment optoins for MG

pharmacology (anticholinesterase drugs, corticosteroids, immmunosuppressives) thymectomy (remove thymus gland) plasmapheresis (removal of abnormal antibodies) immunoglobin (IVIg therapy to reduce autoimmune response

myathenis gravis PT implications management of symptoms

- exercise intensity, duration strategy to improve sx and function - every individual is different - medically managed MG before exercise prescription; - no exercise = energy conservation, transfers, fall prevention - exercise to elevates baseline function

exercise for stable MG pts

energy conservation medication at peak dose large proximal muscle short duration - HR no greater than 30bpm from baseline upper body ergometer, stationary bike, large ms groups posture exercise

what is dementia

an acquired decline in intellectual function and memory - loss of social independence, symptoms progress over months and years

three types of dementia

alzheimers lewy body dementia frontotemporal dementia

what is lewy body dementia

intracellular accumulation of Lewy bodies in the neurons mainly in the cortex

what is frontotemporal dementia

deposition of proteins in the frontal and temporal lobes; early personality and behavior changes and aphasia

causes of dementia

affects 5-20% age 65+, incidence increases with age alzheimers 50% of cases multiple cerebral infarcts (2nd most common cause) dementia with lewy bodies alcoholism

alzheimers disease

slow progressice disorder od the CNS begins w impairments of learning and recent memory progresses to anomia, aphasia, and acalculia (loss of employability)

symptoms and characteristics of alzheimers

spatial disorientation and apraxia ( pts become lost easily and difficulty cooking, cleaning and self care) short shuffling steps, flexed posture,social disconnect, aphasia

pathogenesis of alzheimers

extracellular aggregates of amyloid plaques intracellular neurofibrillary tangles

how many people globally living w Dementia

47 Mill

risk factors of AD

age is a major risk factor 3 major symptoms; memoru function, brain atrophy, accumulations of amyloid protein

amyloid plaques =

= neuron death and inflammation

alzheimers symptoms

confusion w time and locatoin withdrawal from social activities difficulty completing tasks, solving problems, w words misplacing items memory loss poor judgement trouble w images and spaces

what percent of alzheimers cases accounts for dementia cases

60-80%